Vascular cognitive impairment (VCI) is a progressive cognitive impairment caused by cerebrovascular disease or vascular risk factors. It is the second most common type of cognitive impairment after Alzheimer's disease. The pathogenesis of VCI is complex, and neurovascular unit destruction is one of its important mechanisms. The neurovascular unit (NVU) is responsible for combining blood flow with brain activity and includes endothelial cells, pericytes, astrocytes and many regulatory nerve terminals. The concept of an NVU emphasizes that interactions between different types of cells are essential for maintaining brain homeostasis. A stable NVU is the basis of normal brain function. Therefore, understanding the structure and function of the neurovascular unit and its role in VCI development is crucial for gaining insights into its pathogenesis. This article reviews the structure and function of the neurovascular unit and its contribution to VCI, providing valuable information for early diagnosis and prevention.

The glymphatic/lymphatic system of the brain has been an important discovery in the field of neuroscience in recent years. As the "waste clearance network" of the central nervous system, it clears metabolic products and neurotoxic substances through the cerebrospinal fluid–interstitial fluid circulation, which is crucial for maintaining the homeostasis of the intracerebral environment and plays important roles in learning, memory and other advanced cognitive functions. The glymphatic/lymphatic system is crucial for the clearance of beta-amyloid and tau proteins, and thus the abnormal function of this system has been confirmed to be closely related to the pathological mechanisms of various diseases associated with cognitive impairment, such as Alzheimer's disease (AD), Parkinson's disease (PD), and vascular dementia. The physiological function of this system is influenced by a variety of factors, especially when it is relatively active during sleep. The application of noninvasive imaging techniques to assess glymphatic/lymphatic system function has facilitated the development of clinical research. Therefore, a focus on the role of the cerebral glymphatic/lymphatic system in cognitive impairment and an understanding of its relationship with cognitive impairment from a new perspective are of great scientific and clinical importance.

Recently, a wealth of information has emerged connecting the activation of the NLRP3 (NOD-like receptor family pyrin domain-containing 3) inflammasome to stroke pathogenesis, although the exact influence of the NLRP3 inflammasome on stroke is still in the stage of preliminary study and is awaiting further confirmation. In this paper, we will review the structure, assembly and activation of the NLRP3 inflammasome and its expression in the neurovascular units and will speculate on its possible roles in neurovascular injury post-stroke. Evidence on this topic suggests that targeting NLRP3-mediated inflammation at multiple levels may provide a new therapeutic strategy to prevent the deterioration of neurovascular units after stroke. However, many aspects of the biological link between the NLRP3 inflammasome and stroke remain ill-defined or even completely unknown. As fresh insights come to light regarding the NLRP3 inflammasome, the opportunities to develop new therapeutic strategies for stroke patients are expected to improve accordingly.